Evidence map›Paper›PMID 28680392›Full record

ArticleFrontiers in molecular neuroscience2017

Direct Anandamide Activation of TRPV1 Produces Divergent Calcium and Current Responses.

Axel J Fenwick, Daniel K Fowler, Shaw-Wen Wu, Forrest J Shaffer, Jonathan E M Lindberg, Dallas C Kinch, James H Peters

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 48 citations in OpenAlex.

  1. Lipid Activation of a Thalamic GPCR Extends Working Memory Time-scales.bioRxiv : the preprint server for biology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Axel J FenwickDepartment of Integrative Physiology and Neuroscience, Washington State UniversityPullman, WA, United States.
Daniel K FowlerDepartment of Integrative Physiology and Neuroscience, Washington State UniversityPullman, WA, United States.
Shaw-Wen WuDepartment of Integrative Physiology and Neuroscience, Washington State UniversityPullman, WA, United States.
Forrest J ShafferDepartment of Integrative Physiology and Neuroscience, Washington State UniversityPullman, WA, United States.
Jonathan E M LindbergDepartment of Integrative Physiology and Neuroscience, Washington State UniversityPullman, WA, United States.
Dallas C KinchDepartment of Integrative Physiology and Neuroscience, Washington State UniversityPullman, WA, United States.
James H PetersDepartment of Integrative Physiology and Neuroscience, Washington State UniversityPullman, WA, United States.
Washington State University · US

Funding

Asynchronous Glutamate Release in Vagal Afferent to NTS NeurotransmissionR01DK092651 · NIDDK · WASHINGTON STATE UNIVERSITY · PI PETERS, JAMES HENRY · 2012 to 2016
$1.6M
NIDDK NIH HHS R01 DK092651
6 · The paper itself

Abstract

In the brainstem nucleus of the solitary tract (NTS), primary vagal afferent neurons express the transient receptor potential vanilloid subfamily member 1 (TRPV1) at their central terminals where it contributes to quantal forms of glutamate release. The endogenous membrane lipid anandamide (AEA) is a putative TRPV1 agonist in the brain, yet the extent to which AEA activation of TRPV1 has a neurophysiological consequence is not well established. We investigated the ability of AEA to activate TRPV1 in vagal afferent neurons in comparison to capsaicin (CAP). Using ratiometric calcium imaging and whole-cell patch clamp recordings we confirmed that AEA excitatory activity requires TRPV1, binds competitively at the CAP binding site, and has low relative affinity. While AEA-induced increases in peak cytosolic calcium were similar to CAP, AEA-induced membrane currents were significantly smaller. Removal of bath calcium increased the AEA current with no change in peak CAP currents revealing a calcium sensitive difference in specific ligand activation of TRPV1. Both CAP- and AEA-activated TRPV1 currents maintained identical reversal potentials, arguing against a major difference in ion selectivity to resolve the AEA differences in signaling. In contrast with CAP, AEA did not alter spontaneous glutamate release at NTS synapses. We conclude: (1) AEA activation of TRPV1 is markedly different from CAP and produces different magnitudes of calcium influx from whole-cell current; and (2) exogenous AEA does not alter spontaneous glutamate release onto NTS neurons. As such, AEA may convey modulatory changes to calcium-dependent processes, but does not directly facilitate glutamate release.

Indexed as

autonomic reflexescalciumglutamatepermeabilityquantalspontaneousvagus

Identifiers

PMID28680392
PMCPMC5478686
OpenAlexW2670179021

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.